Current Research that You Should Incorporate into Your Mode of Practice Now! Dominick Maino, OD, MEd, FAAO, FCOVD‐A Moderator Featuring the Best of AOA's 2015 Poster Presentations Jun‐27‐2015 8:00AM ‐ 10:00AM Optic Nerve Head Drusen: A Myriad of Presentations Jennifer L. Jones, Sylvia E. Sparrow, Christina Grosshans Validation Study of New LCD‐Based Contrast Sensitivity Testing Method Sarah Henderson, Jeung H Kim, Paul Harris Bilateral Cystoid Macular Edema in Retinitis Pigmentosa and its Management Lindsay T. Gibney An ODE to Optic Disc Edema Kelli Theisen Is Binocular Balancing with Subjective Refraction a thing of the Past? David Geffen Optometry's Meeting 2015 Seattle, Washington

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Dominick Maino, OD, MEd, FAAO, FCOVD‐A
Moderator
Featuring the Best of AOA's 2015 Poster Presentations
Jun‐27‐2015 8:00AM ‐ 10:00AM
3015
Current Research that You Should Incorporate
into Your Mode of Practice Now!
Optic Nerve Head Drusen: A Myriad of Presentations
Jennifer L. Jones, Sylvia E. Sparrow, Christina Grosshans
Validation Study of New LCD‐Based Contrast Sensitivity Testing Method
Sarah Henderson, Jeung H Kim, Paul Harris
Bilateral Cystoid Macular Edema in Retinitis Pigmentosa and its Management
Lindsay T. Gibney
An ODE to Optic Disc Edema
Kelli Theisen
Is Binocular Balancing with Subjective Refraction a thing of the Past?
David Geffen
Cochrane Reviews
http://www.cochrane.org/
… a global independent network of
researchers, professionals,
patients, carers, and people
interested in health…
Cotter SA, Cyert LA, Miller JM, Quinn GE; National Expert
Panel to the National Center for Children’s Vision and Eye
Health. Vision screening for children 36 to <72 months:
recommended practices. Optom Vis Sci. 2015 Jan;92(1):6‐
16.
Clinician’s View of Researchers Researcher’s view of Clinicians

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Poster Session
My Thanks to the AOA Abstract Review Committee
William McAllister, Elizabeth Wyles, Sunny Sanders,
Sarah Hinkley, Christine Allison, Jennifer Harthan, Aurora Denial
90 posters submitted; 50 Posters accepted
Criteria for acceptance similar to those used by other well
respected organizations (clinical aspects emphasized)
Reasons for non‐acceptance:
Did not follow instructions
Data does not support conclusions
Not unique
Poster Session
Please submit Case reports, Case series, Clinical research, etc. in all areas
of optometry for 2016 when the call for abstracts goes out!
Informational Posters Accepted (These also need to be well done and
cannot be a sales pitch for a particular product or service)
The committee judged these posters to be notable and worthy to be
highlighted in this fashion
Questions welcome at the end of each of today’s presentations
Optic Nerve Head Drusen: A Myriad of Presentations
Jennifer L. Jones, Sylvia E. Sparrow, Christina Grosshans
Validation Study of New LCD‐Based Contrast Sensitivity Testing Method
Sarah Henderson, Jeung H Kim, Paul Harris
Bilateral Cystoid Macular Edema in Retinitis Pigmentosa and its
Management
Lindsay T. Gibney
An ODE to Optic Disc Edema
Kelli Theisen
Is Binocular Balancing with Subjective Refraction a thing of the Past?
David Geffen
Optic Nerve Head Drusen:
A Myriad of Presentations
Jennifer L. Jones, O.D.
Sylvia E. Sparrow, O.D., F.A.A.O.
Christina Grosshans, O.D.
Facts about optic nerve head drusen (ONHD)
• Concretions of calcium, nucleic and amino acids,
mucopolysaccharides, and sometimes iron
• Contained within nerve above lamina cribrosa and below Bruch’s
membrane
• ONHD are dynamic: they enlarge slowly throughout a person’s life
•*May* be “buried” in young patients (closer to
lamina cribrosa)
Facts, cont.
• Epidemiology:
• 1% of general population
• More common in Caucasian and female patients
• Autosomal dominant with incomplete penetrance
• Associated conditions: pseudoxanthoma elasticum, RP, angioid streaks
• Signs:
• 75‐85% bilateral
• Yellowish deposits on/around ONH
• ONH margins may be distorted and indistinct
• Loss of cup

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Facts, cont.
• Symptoms:
• Typically asymptomatic
• Transient visual obscurations (8.3%)
• Possible VF defects (enlarged blind spot, arcuate scotoma, and peripheral
defects)
• *Possible* VA loss in association with juxtapapillary CNV
• Complications:
• As drusen enlarge, nerve fibers and vascular supply may be compressed,
leading to VF defects, vascular occlusion, and hemorrhage
• Ex: Retinal vein occlusion, retinal artery occlusion (typically in conjunction with systemic
HTN, migraines, oral contraceptive use), and AION
Facts, cont.
• Treatment:
• None (for drusen itself)
• Monitor with VF, OCT, IOP check
• If VF defect is present, may lower IOP with topical
medications to prevent progression
• If CNV is present, treatment may be needed if central
acuity is threatened
Clinical differences between papilledema and ONHD
Papilledema ONHD
ONH appearance Hyperemic, ill‐defined Lumpy bumpy, ill‐defined
SVP Varies Varies
Peripapillary lesions CWS, hemes, venous congestion Abnormal retinal vasculature
VA impairment Affected in later stages Rare
VF defects Likely* Possible*
Systemic symptoms Headache, nausea, vomiting Absent
ONH calcification Absent Detected with imaging
ONH autofluorescence Absent Present especially if superficial
J Clin Neurol.
2012 Jun; 8(2):
151–154.
Patient 1
MT – 5 year old Caucasian female
• CC: Follow‐up on buried ONHD OU diagnosed 3
months prior
• POcHx: Accommodative esotropia
• PMHx: Unremarkable
• Height/Weight: 3’2”, 45 lbs.
• Medications: None reported
• Allergies: NKDA
Patient 1, cont.
•VA cc: 20/25+2 OD, 20/25+2 OS with +4.50 sph
OD, OS
•Color: “Normal” OD, OS
• Waggoner method
•EOMs: FROM OU
• (‐)pain, (‐)diplopia
•CVF: FTFC OD, OS
•PERRL (‐)APD OD, OS
Patient 1, cont.
•Anterior Seg.: Unremarkable OD, OS
•IOP: 17 mmHg OD, 16 mmHg OS (Icare)
•Posterior Seg.:
• ONH OD, OS: “lumpy” appearance, well perfused,
no obscuration of vessels at margins
• C/D ratio: 0.10R OD, OS
• All else was unremarkable

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Patient 1: ONH OD Patient 1: ONH OS
Patient 1: Red‐free ONH OD Patient 1: Red‐free ONH OS
Patient 1: B‐scan OD, OS Patient 1: B‐scan OD, OS

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Patient 1: OCT OD, OS
Patient 1, cont.
•Assessment:
• 1. Buried ONH drusen OU
•Plan:
• 1. Mother educated on condition; monitor in 6
months
Patient 2
JP – 13 year old Hispanic male
• CC: Pt. presented with h/o mild headaches twice a
week; mother reported pt. plays a lot of video games
• POcHx: Unremarkable
• PMHx: Unremarkable
• Height/Weight: Noncontributory
• BP: 92/57 mmHg
• Medications: None reported
• Allergies: Eggs
Patient 2, cont.
• VA cc: 20/15 OD, OS with +2.50‐3.50X180 OD, +1.25‐2.00X170 OS
• Color: 6/6 pass OD, OS
•HRR
• EOMs: FROM OU
•(‐)pain, (‐)diplopia
• CVF: FTFC OD, OS
• PERRL(‐)APD OD, OS; 5‐3 mm OD, OS
• Anterior Seg.: Unremarkable OD, OS
• IOP: 13 mmHg OD, 14 mmHg OS (Goldmann)
• Posterior Seg.:
• ONH OD: pink, perfused, distinct margins, (+)SVP
• ONH OS: hyperemic, indistinct margins (not noted
previously), (‐)SVP
• C/D ratio: 0.20R OD, 0.1R OS
• All else was unremarkable
Patient 2, cont.
Patient 2: ONH OD, OS

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Patient 2: ONH OD, OS
Patient 2: B‐scan OD, OS
Patient 2: B‐scan OD, OS
Patient 2:
HVF OD, OS
Patient 2: OCT OD, OS
Patient 2, cont.
•Assessment:
•1. Buried ONH drusen OS>OD
•Plan:
•1. Pt. and mother educated on condition;
monitor in 6 months

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Patient 3
TT – 14 year old AA female
• CC: Blur at distance with habitual Rx for 1 month
• POcHx/PMHx: Pt. had h/o headaches 2‐3 yrs. prior and was
diagnosed with pseudopapilledema. At that time, she took
Diamox 250 mg tid for 1 month and then discontinued.
• Height/Weight: 5’3”, 160 lbs.
• BP: 108/77
• Medications: None reported
• Allergies: NKDA
Patient 3, cont.
• VA cc: 20/20 OD, OS with ‐2.50 sph OD, ‐1.75‐
1.00X005 OS
• EOMs: FROM OU
•(‐)pain, (‐)diplopia
• CVF: FTFC OD, OS
• PERRL(‐)APD OD, OS; 6‐4 mm OD, OS
Patient 3, cont.
• Anterior Seg.: Unremarkable OD, OS
• IOP: 20 mmHg OD, 19 mmHg OS (NCT)
• Posterior Seg.:
• ONH OD, OS: irregular, elevated, scalloped‐like
margins 360o, no vessel obscuration at margins,
“lumpy” appearance
• C/D ratio: 0.10R OD, OS
• Vessels: tortuosity OU
• All else was unremarkable
Patient 3: ONH OD, OS
Patient 3: ONH OD, OS Patient 3: Red‐free ONH OD

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Patient 3: Red‐free ONH OS Patient 3: B‐scan OD
Patient 3: B‐scan OS
Patient 3:
HVF OD,
OS
Patient 3: OCT OD, OS
Patient 3, cont.
•Assessment:
•1. ONH drusen OU
•Plan:
•1. Pt. and mother educated on findings and
condition. RTC 1 year for annual exam and
HVF or ASAP if any changes.

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Patient 4
DB – 25 year old Hispanic female
• CC: Annual examination
• POcHx: h/o pseudotumor cerebri diagnosed in Venezuela approx. two years prior
Unremarkable MRI four years ago for “soft spot in skull;” never had lumbar puncture;
was told to lose weight and also prescribed medicine for two weeks that she did not
tolerate
• PMHx:
• Headaches—takes Aleve bid daily; awakens with headache and rarely goes away
• Weight has varied throughout teenage years (180s‐240s)
• Height/Weight: 5’6”, 243 lbs.
• BP: 113/84 mmHg
• Meds: Birth control pill from Venezuela—inconsistent use
• Allergies: NKDA
Patient 4, cont.
• VA cc: 20/20 OD, OS with ‐0.25‐1.00X105 OD and ‐
0.25 sph OS
• Color: 10/10 OD, OS
•Ishihara
• EOMs: FROM OU
• CVF: FTFC OD, OS
• PERRL (‐)APD
Patient 4, cont.
• Anterior Seg.: Unremarkable OU
• IOP: 20, 20 mmHg OD, OS
• Posterior Seg.:
•ONH OD, OS: “lumpy” appearance, well
perfused, no obscuration of vessels at
margins
•C/D ratio: no physiological cupping
•All else was unremarkable
Patient 4: ONH OD
Patient 4: ONH OS Patient 4: B‐Scan OD OD, OS

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Patient 4: B‐scan OS Patient
4: HVF
OD, OS
Patient 4: OCT OD, OS
Patient 4, cont.
•Assessment
•1. ONH drusen OU
•Plan
•Pt. education; monitor yearly
Patient 5
JS – 42 year old Patient Caucasian male
• CC: Blur at near > distance without correction
• POcHx: LEE 1 yr. prior; told nerves were “abnormal”
• PMHx: Negative
• Height/Weight: 5’9”, 183 lbs.
• BP: 123/59 mmHg
• Medications: None reported
• Allergies: NKDA
Patient 5, cont.
•VA cc: 20/20 OD, OS with +0.25‐
0.75X090 OD, plano OS and +1.25 add
(20/20)
•EOMS: FROM OU
•CVF: FTFC OD, OS
•PERRL (‐)APD

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Patient 5, cont.
• Anterior Seg.: Unremarkable
• IOP: 14 mmHg OD, OS (Goldmann)
• Posterior Seg.:
•ONH OD, OS: congested, “bumpy”
margins
•C/D ratio: <0.1R OD, OS
•Vessels: tortuosity OU
•All else was unremarkable
Patient 5: Posterior Pole OD
Patient 5: Posterior Pole OS Patient 5: Red‐Free Posterior Pole OD
Patient 5: Red‐Free Posterior Pole OS Patient 5: B‐scan OD

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Patient 5: B‐scan OD, OS
Patient 5: OCT OD, OS
Patient 5, cont.
•Assessment
•1. ONH drusen OU with vessel tortuosity
•Plan
•1. Pt. education; monitor yearly
Patient Comparison
Pt. 1 Pt. 2 Pt. 3 Pt. 4 Pt. 5
Age 5 13 14 25 42
Race Caucasian Hispanic AA Hispanic Caucasian
Sex Female Male Female Female Male
Visible ONHD No No Yes Yes Yes
Confirmed with
B‐scan
Yes No Yes Yes Yes
In summary…
• Most patients have no associated predisposing ocular or systemic
conditions
• Patients are usually asymptomatic; visual acuity is generally well
preserved but visual field defects may be present and increase over
time
• Proper diagnosis is important to avoid unnecessary testing
• ONHD are usually buried in children and become more superficial in
adults
• Tests helpful for diagnosis include funduscopy, ultrasonography,
CT/MRI, fluorescein angiography, and OCT
• Regular monitoring is important to rule out accompanying disorders
References • 1. Auw‐Haedrich, C., et al. Optic Disk Drusen. Survey of Ophthalmology. 2002 Dec; 47(6): 515‐532.
• 2. Gili, P., et al. Using autofluorescence to detect optic nerve head drusen in children. J AAPOS 2013; 17: 568‐571.
• 3. Grippo T., et al. Optic disc drusen: practical implications and management. Glaucoma Today. Jan/Feb 2012. Available at:
http://bmctoday.net/glaucomatoday/2012/02/article.asp?f=optic‐disc‐drusen. Accessed 5/13/15.
• 4. Johnson, L., et al. Differentiating Optic Disc Edema From Optic Nerve Head Drusen on Optical Coherence Tomography. Arch
Ophthalmol 2009;127(1):45‐49.
• 5. Katz, B., et al. Visual Field Defects and Retinal Nerve Fiber Layer Defects in Eyes with Buried Optic Nerve Drusen. Am J Ophthalmol
2006: 141: 248‐253.
• 6. Kaushal, K., et al. Differentiating Mild Papilledema and Buried Optic Nerve Head Drusen Using Spectral Domain Optical Coherence
Tomography. Ophthalmology April 2014; 121(4): 959‐963.
• 7. Laul, A., et al. A Detailed Look at Optic Nerve Anomalies. Review of Optometry. 9/15/14. Available at:
http://www.reviewofoptometry.com/content/c/50440/. Accessed 5/13/15.
• 8. Lee, K., et al. Differentiation of Optic Nerve Head Drusen and Optic Disc Edema with Spectral‐Domain Optical Coherence Tomography.
Ophthalmology 2011; 118: 971‐977.
• 9. Mansour, A., et al. Racial Variation of optic nerve diseases. Neuro‐ophthalmology 1991: 11(6): 319‐323.
• 10. Merchant, K., et al. Enhanced Depth Imaging Optical Coherence Tomography of Optic Nerve Head Drusen. Ophthalmology 2013;
120: 1409‐1414.
• 11. Morris, R., et al. Advanced visual field loss secondary to optic nerve head drusen: Case report and literature review. Optometry
2009; 80: 83‐100.
• 12. Patel, V., et al. Optic Nerve Drusen. EyeRounds.org. August 14, 2007; Available at: http://www.EyeRounds.org/cases/72‐Optic‐
Nerve‐Drusen‐Visual‐Field‐Loss.htm. Accessed 5/20/15.
• 13. Sahin, A., et al. Bilateral Optic Disc Drusen Mimicking Papilledema. J Clin Neurol 2012 Jun; 8(2): 151–154.
• 14. Sato, T., et al. Multimodal Imaging of Optic Disc Drusen. Am J Ophthalmol 2013; 156: 275‐282.
• 15. Thurtell, MJ., et al. Optic nerve head drusen in black patients. J Neuroophthalmol March 2012; 32(1): 13‐16.
• 16. Wong, S., et al. The Clinical Validity of the Spontaneous Retinal Venous Pulsation. J Neuroophthalmol March 2013; 33(1): 17‐20.

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Questions? Questions?
1a) Which is more common with optic disc drusen‐‐visual acuity
impairment or visual field defects?
1b) Are you more likely to have VF defects with buried ODD
identified by ultrasonography or visible ODD?
1c) What are the most common VF defects?
2) Why can’t ultrasonography detect ODD in young patients?
3) What is the most important differential diagnosis and why?
Validation study of new LCD based contrast
sensitivity testing method
Sarah Henderson, BS
Paul Harris, OD, FCOVD, FACBO, FAAO, FNAP
Jeung Kim, PhD, OD
Southern College of Optometry
Memphis, TN 38104
• Why is CS important?
• Can assess different aspects of ocular
conditions that go well beyond standard
measures of visual acuity (VA)
• Gives more comprehensive understanding
of visual function
• Several ocular conditions can contribute
to poor CS
Contrast Sensitivity (CS)
CS Tests
• Pelli‐Robson
• Contrast threshold for a fixed letter size
• Bailey‐Lovie high and low‐contrast chart
• Optotype threshold for a fixed contrast level
• Vistech
• 5 different spatial frequency levels to obtain a CS curve
• Limited application
•Cataracts and other media opacities
•Amblyopia
•Retinal dystrophy and degeneration
•Optic neuropathy (e.g. glaucoma)
•Vascular conditions (e.g. diabetic
retinopathy)
Lists of Ocular Conditions

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• Used on a liquid‐crystal‐display (LCD)
monitor
• Manipulation of contrast level with
different optotype sizes
• Two types of target: Sloan letters, sine
wave grating
Harris Contrast Test (M&S Smart System®) Harris Contrast Test (M&S Smart System®)
Harris Contrast Test (M&S Smart System®)
• To assess the validity of acuity thresholds on a fixed
contrast level on the Harris chart as compared to the
Bailey‐Lovie low contrast chart.
• To validate the use of the Harris chart in establishing
one’s contrast sensitivity curve across varying acuity
levels.
Purpose of Study
•53 healthy adults were
examined
•Inclusion criteria:
•BCVA of 20/20 or better
•Absence of systemic and/or
ocular conditions that can
decrease CS
•Mean age: 29 (+/‐10.5 years)
Methods
• Initial BCVA measured on high‐contrast Bailey‐
Lovie chart
• Low contrast acuity threshold measured on
low‐contrast Bailey‐Lovie chart
• Low contrast acuity threshold measured on
Harris contrast chart at fixed 18% Weber
contrast level
• Contrast thresholds measured at 20/400,
20/200, 20/100, 20/50, 20/40 and 20/30 Sloan
letters
Methods (Cont’d)

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•Low contrast Bailey‐Lovie logMAR:
• ‐0.006 (+/‐ 0.11)
• VA equivalent: 20/19.725
•Harris equivalent logMAR:
• ‐0.0038 (‐0.0038 +/‐ 0.09)
• VA equivalent 20/19.825
•No statistically significant different
(p=0.455)
Results Results (Cont’d)
1
1.1
1.2
1.3
1.4
1.5
1.6
1.7
20/400 20/200 20/100 20/50 20/40 20/30
Contrast Thresholds
a a a
b
c
d
LogCS
Sloan letter sizes
•Demonstrated the utility and efficacy of the
Harris contrast chart (M&S Technologies) as
compared to traditional tests (Bailey‐Lovie low
contrast chart)
•Overall CS function readily obtainable
Conclusion
• M&S Technologies
• Dr. Patricia Cisarik, OD, PhD
• Summer research fellowship at Southern College of
Optometry
• Any questions
• Email: jkim@sco.edu
Acknowledgement
• Bex, P, Pelli, DG. Measuring Contrast Sensitivity. Vision Research. 90
(2013) 10–14.
• Bonette, L, Elliott, DB, Whitaker, D. Differences in the legibility
of letters at contrast threshold using the Pelli‐Robson chart.
Ophthal. P hysiol. Opt. 10 (1990) 323‐326.
• Bullimore, MA, Elliott, DB. Assessing the Reliability, Discriminative
Ability and Validity of Disability Glare Tests. Investigative
Ophthalmology & Visual Science. 34 (1993) 108‐19.
• I.L. Bailey, J.E. Lovie‐Kitchin / Vision Research 90 (2013) 2–9.
References: Questions?
Why is contrast sensitivity important?
Because a high contrast Dominick Maino looks so much better than
low contrast Maino!

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Questions?
1. What benefits does the Harris chart have over other
standard contrast charts?
2. Is it commercially available?
3. How would you incorporate it into a routine
examination?
Bilateral Cystoid Macular Edema
in Retinitis Pigmentosa and its
Management
Lindsay T. Gibney OD, FAAO
Resident, Omni Eye Specialist Baltimore
Retinitis Pigmentosa
• A group of inherited disorders resulting in progressive degeneration and
dysfunction of photoreceptors and RPE.
• Hallmark symptoms include difficulty with night vision and progressive
peripheral visual field loss.
• Retinal signs include bone spicules, mottling and granularity of the RPE,
attenuated vessels, waxy pallor of optic nerve head.
• Generally thought of as affecting peripheral vision, but central vision
often affected in advanced disease and loss can occur early on from…
• PSC Cataracts
• Central Retinal Degeneration
• Macular Edema
Genetics
• May be inherited in many different patterns including, autosomal
dominant, autosomal recessive and X‐linked.
• Simplex RP: When no other affected family member can be identified.
Large percentage are likely autosomal recessive.
• May be typical (non‐syndromic) or complicated (syndromic).
• Many different genetic mutations are associated with RP. Rhodopsin
mutations are an example of a common genetic mutation leading to RP.
• Those with the autosomal dominant pattern are more likely to retain
good vision late in life compared to recessive or x‐linked.
“Worsening central vision loss.”
CC: 27 W M with complaints of significant decrease in central vision about
2 days prior. Recently moved to the area and was seeing a retina specialist
prior to relocating. Diagnosed with RP by last provider, but had previously
been told had macular degeneration.
Ocular Hx: Retinitis Pigmentosa, No known ocular procedures
Medical Hx: Overall healthy
Medications: dorzolamide 2% bid OU ‐ discontinued
Last Eye Exam: About 2 months ago
Exam findings
Entrance Testing OD OS
BCVA 20/200 20/400
Pupils PERRL, (‐) APD PERRL, (‐) APD
Confrontation Visual Field FTFC FTFC
Ocular Motility EOMI
Muscle Balance Ortho on penlight
IOP 18 mmHg (Applanation) 16 mmHg (Applanation)
Dilation 1% Tropicamide & 2.5% phenylephrine OU @ 1:03 pm

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External Exam OD OS
Adnexa Normal Normal
Lids Normal Normal
Conjunctiva Clear Clear
Cornea Clear Clear
Anterior Chamber Deep & Quiet Deep & Quiet
Iris Normal pupil size & shape Normal pupil size & shape
Lens Clear Clear
Internal Exam OD OS
Vitreous (+) vitreous cells (+) vitreous cells
Optic Disc 0.4, no edema, no vascularization,
good color
0.4, no edema, no vascularization,
good color
Macula Macular thickening, NO FLR Macular thickening, NO FLR
Vessels 2/3 ratio w/o tortuosity 2/3 ratio w/o tortuosity
Periphery Flat & attached 360, RPE
Hypertrophy/mild Bone spicules
Flat & attached 360, RPE
Hypertrophy/mild Bone spicules
Macular Edema in Retinitis Pigmentosa
Exact mechanism unclear, likely multifactorial
‐ Low grade inflammation leading to breakdown of blood‐retinal barrier
‐ Decreased efficiency of RPE
‐ Antiretinal antibodies; antienolase and anticarbonic anhydrase
‐ Epiretinal membranes
‐ Pseudophakic CME, RP patients more susceptible to inflammation
Rate of CME found to be 32% in at least one eye on SD‐OCT, even in patients
with no fundoscopic evidence. 1
May be as high as 70% of patients with RP. 2
CAIs for Macular Edema in RP
• Mechanism of Action: Main effect is likely increase passage of fluid through
the RPE. May also improve extrafoveal sensitivity resulting in subjective
improvement.
• Topical vs. Oral: Initial studies showed that oral was more efficacious. May not
have been long enough. May take month to get a response.
• Leakage on FA vs. no leakage response to CAI: Macular edema in RP mostly
does not show leakage on FA and is less responsive to current therapies for
macular edema.
• Efficacy of CAIs: Most effective option based on the current literature. 20‐
55.6% success rates/improvement in acuity.1
• Other possible options
• Steroids
• Intravitreal (Ozurdex, Allergan)
• Topical?
• NSAIDs

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Current Considerations
1) OCT for patients with known RP
2) Also VF – Goldmann or Octopus – recommended at least every 2 years to monitor
field of vision for driving
3) Other testing: FA, ERG, microperimetry and autofluorescence
4) Syndromic RP may need consults with other practitioners – e.g. Usher Syndrome
5) Genetic Counseling – May help determine prognosis and guide therapy.
6) Low Vision consult
7) Psychological Counseling
Potential Adverse Factors
• Smoking
• Light
• UV protection
• Blue light filtering?
• Bright flash photography?
• Medications
• Isoretinin
• Vitamin E
• Viagra
Future
•Vitamin therapy
•Gene & Stem Cell therapy
•Retinal devices
Vitamin Therapy
• Vitamin A
• May slow progress of RP – effects modest, 2%
• Very high dosage, 15,000 IU/day– monitor for toxicity, baseline and annual liver function tests
• Lower dosages are known to cause birth defects – careful with females
• Response may be genotype dependent – may need to be guided by genotyping
• DHA
• Trial found it to enhance the benefits of Vitamin A therapy for up to 2 years, not found to be
beneficial alone.
• Patients with X‐linked RP found to have lower levels of DHA.
• 400mg‐1200mg/day
• Lutein
• Thought to be beneficial. Has shown lessened mid‐peripheral field loss when taken with
Vitamin A.
• 12‐20mg/day2‐4
Gene & Stem Cell Therapy
Gene Therapy
• Either add function or block function
• May only be preventative, only useful for early disease
• Limited historically by non‐specific transfection
• Typically uses Adeno‐associated virus (AAV) delivery
• Carries a limited amount of DNA
Stem Cell Therapy
• Replaces cells lost due to the disease
• Transplanted photoreceptors must be integrated into the retina, cannot use
mature photoreceptors5
• 3D retinal layer grown in lab recently6
Retinal Devices
• May be sub‐retinal or epiretinal
• Argus II (Second Sight)
• Epiretinal
• FDA approved in February 2013
• Approved for “Severe” Retinitis Pigmentosa: 25 yrs or older
with bare or NLP vision from advanced RP
• Cost ~ $145,0007

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Bibliography
1) Ryan S, Schachat A, Wilkinson C, Hinton D, Sadda S, Wiedemann P. Retina. Elsevier
Health Sciences; 2013.
2) Gallemore R, Shyu A, Heckenlively, J. Retinitis Pigmentosa: Optimizing Care for Your
Patients. New Retina MD. Fall 2013.
3) Telander D. Retinitis Pigmentosa Treatment & Management. Medscape Reference.
Updated Feb 17, 2015. http://emedicine.medscape.com/article/1227488‐
treatment#showall. Accessed May 26,2015.
4) Rayapudi S, Schwartz SG, Wang X, Chavis P. Vitamin A and fish oils for retinitis
pigmentosa. The Cochrane database of systematic reviews. 2013;12:CD008428.
doi:10.1002/14651858.CD008428.pub2.
5) Lin M, Tsai Y, Tsang S. Emerging Treatments for Retinitis Pigmentosa. Retinal Physician,
Volume: 12 , Issue: March 2015, page(s): 52‐55, 70.
6) Roth M. Can embryonic stem cells help stop blindness? Pittsburgh Post‐Gazette. May 24,
2015. http://www.post‐gazette.com/news/health/2015/05/24/Can‐embryonic‐stem‐cells‐
help‐stop‐blindness/stories/201505250008. Accessed May 26, 2015.
7) Castillo M. FDA‐approved bionic eye Argus II aims to restore some vision in the blind.
CBS News. October 7, 2013. http://www.cbsnews.com/news/fda‐approved‐bionic‐eye‐
argus‐ii‐aims‐to‐restore‐some‐vision‐in‐the‐blind/. Accessed May 26,2015.
Questions?
Questions?
1) Why is macular edema in RP patients
unresponsive to anti‐VEGF therapy?
2) What are predictors of visual loss in RP?
3) What is the recommended dosage for CAI
therapy?
An ODE to Optic Disc Edema
Kelli Theisen, O.D.
Primary Care and Ocular Disease Resident
Illinois College of Optometry/Illinois Eye Institute
AOA‐ Optometry’s Meeting 2015
Case History
• 32 AAM: IEI Urgent Care Referral “Papilledema OS”
• CC: peripheral blur
• HPI:
• OS
• X 2 weeks
• Clear central vision
• (+) dulling of colors
• PO/MHx: unremarkable
• SHx: former smoker, occasional EtOH
Clinical Exam
OD OS
20/20‐1 VA 20/20‐1
FTFC CVF FTFC
FULL, (+) discomfort in right
gaze
EOMs FULL, (+) discomfort in right
gaze
E(3)RRL Pupils E(3)RRL, 1+ APD
100% Red Cap Desaturation 80%
K scar SLE K scar
See Photo DFE See Photo

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OD OS
Differential Diagnoses
 Anterior ischemic optic neuropathy
 Nonarteritic
 Arteritic
 Optic neuritis
 Demyelinating
 Infectious/infiltrative
 Compressive lesion
 Toxic optic neuropathy

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NA‐AION
• Age 61 ± 12
• (+) Disc Hemes
• Altitudinal VF loss
• Minimal color loss
• Painless
• Disc at risk
• Systemic RFs
Optic Neuritis
• Age 18‐45
• (‐) Disc Hemes
• Variable VF loss
• Substantial color loss
• Pain on EOMs
• Systemic causes
Leading Differentials
NA‐AION
• Age 61 ± 12
• (+) Disc Hemes
• Altitudinal VF loss
• Minimal color loss
• Painless
• Disc at risk
• Systemic RFs
Optic Neuritis
• Age 18‐45
• (‐) Disc Hemes
• Variable VF loss
• Substantial color loss
• Pain on EOMs
• Systemic causes
Leading Differentials
NA‐AION
• Age 61 ± 12
• (+) Disc Hemes
• Altitudinal VF loss
• Minimal color loss
• Painless
• Disc at risk
• Systemic RFs
Optic Neuritis
• Age 18‐45
• (‐) Disc Hemes
• Variable VF loss
• Substantial color loss
• Pain on EOMs
• Systemic causes
Leading Differentials
http://www.reviewofoptometry.com/content/c/50440/ http://www.ophthalmicphotography.info/website/disc/neuritis.html
T1 T2 FLAIR T2 post gadolinium with fat suppression

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LABS and CXR
Lab Test Value √ / X
Syphilis Screen (EIA) Non‐reactive √
Diabetes
Glucose 101 √
HbA1c 5.4 √
Lipid Panel
Cholesterol 167 √
Triglycerides 61 √
HDL 54 √
LDL 101 √
Angiotensin Converting Enzyme 14 √
Chest XR ‐ Possible mild R and L hilar lymphadenopathy ?
Chest CT ‐ Calcified nodule c/w granuloma; no hilar adenopathy ?
NA‐AION
• Age 61 ± 12
• Sudden, painless VA loss
• ONH edema, (+) hemes
• Systemic risk factors
• Diabetes
• Hypertension
• Blood loss
• Hyperlipidemia
• Sleep apnea
• Migraine
• Smoking
• PDE‐5 inhibitors
• ONH risk factors
• “Disc at risk”
• Drusen
• Edema
• Defective circulatory auto‐
regulation
Blood supply to ONH
• CRA
• SPCA
• Pial plexus
Ischemia of
ONH
Axoplasmic
flow stasis
Axonal
swelling
Disc at risk
Vascular
compression
NA‐AION
NA‐AION Treatment?
 Ischemic Optic Neuropathy Decompression Trial
 Sergott 1989
 .
 Systemic steroids
 Aspirin
 Triamcinolone
 Avastin
Observe ONDS
VA ↑ 43% 33%
VA ↓ 12% 24%
NA‐AION Management
 If ≥ 50 YO
 ESR
 CRP
 Fluorescein Angiography
 Identify vascular risk factors
 Monitor
 Resolution of edema
 RNFL loss
 Risk of recurrence

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Initial visit 4 months later
Initial visit 4 months later
Summary
• Be suspicious of GCA
• Differentials in atypical presentations
• PCP coordination
• Vision on presentation
• Color plates vs red cap
Literature ReviewedArnold AC, Costa RMS, Dumitrascu OM. The spectrum of optic disc ischemia in patients younger than 50 years (an American Ophthalmological Society Thesis). Trans Am
Ophthalmol Soc 2013; 111: 93‐118.
Atkins EJ, Bruce BB, Newman NJ, Biousse V. Treatment of Nonarteritic Anterior Ischemic Optic Neuropathy. Surv Ophthalmol 2010; 55(1): 47‐63.
Bender B, Heine C, Danz S, Bischof F, Reimann K, Bender M, Nagele T, Ernemann U, Korn A. Diffusion Restriction of the Optic Nerve in Patients With Acute Visual Deficit. J. Magn.
Reson. Imaging 2014; 40: 334‐340.
Contreras I, Noval S, Rebolleda G, Munoz‐Negrete FJ. Follow‐up of Nonarteritic Anterior Ischemic Optic Neuropathy with Optical Coherence Tomography. Ophthalmology 2007;
114: 2338‐2344.
Deramo VA, Sergott RC, Augsburger JJ, Foroozan R, Savino PJ, Leone A. Ischemic Optic Neuropathy as the First Manifestation of Elevated Cholesterol Levels in Young Patients.
Ophthalmology 2003; 110: 1041‐1045.
Friedland S, Winterkorn JMS, Burde R. Luxury Perfusion Following Anterior Ischemic Optic Neuropathy. Journal of Neuro‐Ophthalmology 1996; 16(3): 163‐171.
Ischemic Optic Nueropathy Decompression Trial Research Group. Ischemic Optic Neuropathy Decompression Trial: twenty‐four– month update. Arch Ophthalmol 2000; 118: 793‐
798.
Hayreh SS. Ischemic optic neuropathies—where are we now? Graefes Arch Clin Exp Ophthalmol 2013; 251: 1873‐1884.
Hayreh SS. Management of ischemic optic neuropathies. Indian J Ophthalmol 2011; 59 (2): 123‐136.
Hayreh SS, Zimmerman MB. Nonarteritic Anterior Ischemic Optic Neuropathy: Natural History of Visual Outcome. Ophthalmology 2008;115 (2): 298‐305.
Hayreh SS, Zimmerman MB. Optic disc edema in non‐arteritic anterior ischemic optic neuropathy. Graefe’s Arch Clin Exp Ophthalmol 2007; 245: 1107‐1121.
He M, Cestari D, Cunnane MB, Rizzo JF. The Use of Diffusion MRI in Ischemic Optic Neuropathy and Optic Neuritis. Seminars in Ophthalmology 2010; 25(5‐6): 225‐232.
Laties, AM. Vision Disorders and Phosphodiesterase Type 5 Inhibitors, A Review of the Evidence to Date. Drug Safety 2009; 32(1): 1‐18.
O’Neill EC, Danesh‐Meyer HV, Connell, PP, Trounce IA, Coote MA, Mackey DA, Crowston JG. The optic nerve head in acquired optic neuropathies. Nat Rev Neurol 2010; 6: 221‐
236.
Preechawat P, Bruce BB, Newman NJ, Biousse V. Anterior Ischemic Optic Neuropathy in Patients Younger than 50 Years. Am J Ophthalmol 2007; 144: 953‐960.
Thank You
• Dr. Leonard Messner
• Dr. Stephanie Klemencic
• Dr. Christina Morettin
Questions?

24. 6/16/2015
24
Questions?
1‐ What is the chance of a recurrence of NAION
in the fellow eye?
2‐ How often does a visual field “improve”
following an acute episode of NAION?
3‐ Does the literature suggest any correlated
systemic etiologies for NAION in young
individuals?
Is Binocular Balancing with
Subjective Refraction a thing of the
Past?
David I. Geffen, OD, FAAO
Refraction
•Over 100 years the same method
•Confusing for the patient
•Inaccurate
•Low Tech
20/20 is not Vision Optimized! PSF Refraction Is More Sensitive
• Changes in 0.05D are now noticeable

25. 6/16/2015
25
145 146
147
Patient Responses
• Easier to tell the difference
• High tech
• Less strain
• Feels more accurate
Generates More Accurate Rx
•Subjective refraction – not auto‐refraction
• Rx is at equal or higher level of reliability than a phoropter (unlike
objective wavefront devices)
•Point Spread Function technology attains a
higher level of sensitivity and accuracy
• Patients can discern differences more clearly with PSF than with
Snellen letters
•PSF refines the Rx end point to 0.05D, 5X
better than phoropters
• Provides highest level of visual acuity and contrast
Maximum Plus Maximum Visual Acuity
• Prevention of over‐minussing due to the true perception of the
PSF and the target detail versus using Snellen optotypes which
requires one self to determine their own visual stress point of
smaller and darker.
• With the Vmax system if the patient is over‐minused, the target
simply looks blurry again. This allows for a decrease in the level of
patient frustration by having an un‐ambiguous which yields a higher
level of clinical confidence. Confidence in the refraction was found
to 95% amongst patients achieving identical or better refraction
with the device compared to a manual phoropter
150
[1] Vmax Data of file.

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26
70%
27%
3%
30 Patients Study (Right Eye)
The Difference in Spherical Equivalence Between Binocular
Balanced Phoropter Rx versus PSF Refractor Rx
Equal to or Less than .13D Difference
Greater Than .13D Difference
Greater than .255D Difference
VMax® Systems
152
A Complete Refraction-Lane-in-a-Box
PSF Integra™ PSF Refractor™
Questions? Questions?
1) Do we really need to have an accuracy of 0.05D when we
conduct a refraction?
2.) How does point spread refracting control
accommodative response?
3) Why is point spread refracting more accurate than
standard refracting?
4) I use an automated phropter, why would I consider this?
Any other comments or
questions?
Thank You!